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[心力衰竭的分子基础]

[Molecular bases of heart failure].

作者信息

Rodríguez Pérez José Manuel, Gallardo Guillermo J, Vargas Alarcón Gilberto

机构信息

Departamento de Fisiologia y Grupo de Estudio en Genómica y Proteómica en Enfermedades Cardiovasculares, Instituto Nacional de Cardiología "Ignacio Chávez".

出版信息

Arch Cardiol Mex. 2006 Oct-Dec;76 Suppl 4:S10-7.

PMID:17469331
Abstract

Heart failure (HF) is a complex pathophysiologic state in which delivery of blood and nutrients is inadequate for tissue requirements. HF almost always arises in patients with previous cardiovascular disease such as acute myocardial infarction, atherosclerosis, cardiomyopathy, myocarditis, congenital malformations, or valvular disease. Recently, substantial progress has been made to understand the etiology, pathogenesis, and mechanisms of HF. Several inter-related mechanisms such as oxidative stress, signal transduction, abnormalities in intracellular calcium handling, mitochondrial dysfunction and inherited mutations have been proposed as the triggers of HF.

摘要

心力衰竭(HF)是一种复杂的病理生理状态,在此状态下,血液和营养物质的输送不足以满足组织的需求。HF几乎总是发生在患有先前心血管疾病的患者身上,如急性心肌梗死、动脉粥样硬化、心肌病、心肌炎、先天性畸形或瓣膜疾病。最近,在了解HF的病因、发病机制和机制方面取得了重大进展。几种相互关联的机制,如氧化应激、信号转导、细胞内钙处理异常、线粒体功能障碍和遗传突变,已被提出作为HF的触发因素。

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